Publications by authors named "Jian Yao"

354 Publications

Selective and Efficient Photoinactivation of Intracellular and MRSA with Little Accumulation of Drug Resistance: Application of a Ru(II) Complex with Photolabile Ligands.

J Med Chem 2021 Jun 25;64(11):7359-7370. Epub 2021 May 25.

Key Laboratory of Photochemical Conversion and Optoelectronic Materials, Technical Institute of Physics and Chemistry, Chinese Academy of Sciences, Beijing 100190, P. R. China.

Novel antibacterial agents capable of efficiently sterilizing intracellular and methicillin-resistant (MRSA) but with low cytotoxicity and low resistance development are quite appealing. In this work, three Ru(II) complexes with photolabile ligands were explored to realize such a goal. Complex (5 μM) can inhibit more than 90% growth of /MRSA that has invaded in J774A.1 cells upon visible light irradiation, being much more efficient than vancomycin. In similar conditions, negligible dark- and phototoxicity were found toward the host cells. The bactericidal activity is highly correlated with DNA covalent binding by the Ru(II) fractions generated after ligand photodissociation. Moreover, quickly developed resistance toward vancomycin, while negligible resistance toward complex even after 700 generations was obtained. These appealing results may pave a new way for fighting against intracellular antibiotic-resistant pathogens.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1021/acs.jmedchem.0c02257DOI Listing
June 2021

LncRNA NCK1-AS1 exerts oncogenic property in gastric cancer by targeting the miR-22-3p/BCL9 axis to activate the Wnt/β-catenin signaling.

Environ Toxicol 2021 May 11. Epub 2021 May 11.

Department of Gastroenterology, Jinhu People's Hospital, Huaian, Jiangsu, China.

Long noncoding RNAs (lncRNAs) exert crucial effects on the development of many malignancies, including gastric cancer. Herein, we investigated the role of lncRNA noncatalytic region of tyrosine kinase adaptor protein 1 (NCK1) divergent transcript (NCK1-DT, also known as NCK1-AS1) in gastric cancer. Reverse transcription quantitative polymerase chain reaction demonstrated that NCK1-AS1 exhibited high expression in gastric cancer tissues and cells. In vitro assays including MTT, colony formation, Transwell, wound healing and sphere formation assays indicated that NCK1-AS1 depletion inhibited cell proliferation, migration, invasion and stemness maintenance. Luciferase reporter and RIP assays suggested that NCK1-AS1 functioned as a competitive endogenous RNA (ceRNA) for miR-22-3p to positively modulate BCL9 expression. BCL9 was a target gene of miR-22-3p. According to western blot analysis and TOP/FOP flash assay, NCK1-AS1 activated the Wnt/β-catenin signaling via the miR-22-3p/BCL9 axis. Furthermore, rescue experiments verified that NCK1-AS1 affected cellular processes by activating the Wnt/β-catenin signaling pathway via the miR-22-3p/BCL9 axis. Tumor xenograft model validated that NCK1-AS1 promoted tumor growth in vivo via the Wnt/β-catenin signaling by upregulating BCL9 expression. Overall, NCK1-AS1 functions as an oncogene and promotes gastric cancer progression via the miR-22-3p/BCL9-Wnt/β-catenin signaling pathway.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1002/tox.23160DOI Listing
May 2021

Diagnostic Role of Four-Dimensional Computed Tomography for Preoperative Parathyroid Localization in Patients with Primary Hyperparathyroidism: A Systematic Review and Meta-Analysis.

Diagnostics (Basel) 2021 Apr 7;11(4). Epub 2021 Apr 7.

Department of Radiology, Beijing Luhe Hospital, Capital Medical University, No 82 Xinhua South Road, Tongzhou District, Beijing 101149, China.

We sought to systematically evaluate diagnostic performance of four-dimensional computed tomography (4D-CT) in the localization of hyperfunctioning parathyroid glands (HPGs) in patients with primary hyperparathyroidism (pHPT). We calculated the pooled sensitivity, specificity, positive likelihood ratio (PLR), negative likelihood ratio (NLR), and diagnostic odds ratios (DOR) of 4D-CT on a per-lesion level, as well as pooled sensitivity and positive predictive value (PPV) on a per-patient level with 95% confidence intervals (CIs). Additionally, we plotted summary receiver operating characteristic (SROC) curves and evaluated the areas under the curves (AUC). A total of 16 studies were included in the analysis. Their pooled sensitivity, specificity, PLR, NLR, and DOR of 4D-CT on per-lesion level were 75% (95%CI: 66-82%), 85% (95%CI: 50-97%), 4.9 (95%CI: 1.1-21.3), 0.30 (95%CI: 0.19-0.45), and 17 (95%CI: 3-100), respectively, with an AUC of 81% (95%CI: 77-84%). We also observed heterogeneity in sensitivity (I = 79%) and specificity (I = 94.7%), and obtained a pooled sensitivity of 81% (95%CI: 70-90%) with heterogeneity of 81.9% ( < 0.001) and PPV of 91% (95%CI: 82-98%) with heterogeneity of 80.8% ( < 0.001), based on a per-patient level. Overall, 4D-CT showed moderate sensitivity and specificity for preoperative localization of HPG(s) in patients with pHPT. The diagnostic performance may improve with 4D-CT's promotion to first-line use on a lesion-based level, further research is needed to confirm the results.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3390/diagnostics11040664DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8068020PMC
April 2021

Photo-induced mitochondrial DNA damage and NADH depletion by -NO modified Ru(II) complexes.

Chem Commun (Camb) 2021 Apr;57(34):4162-4165

Key Laboratory of Photochemical Conversion and Optoelectronic Materials, Technical Institute of Physics and Chemistry, Chinese Academy of Sciences, Beijing 100190, P. R. China.

Two mitochondria-localized Ru(ii) complexes with photo-labile ligands were reported to exert one- and two-photon activatable anticancer activity through a dual-function mechanism, i.e. mitochondrial DNA covalent binding after photo-induced ligand dissociation and photo-catalyzed NADH depletion, thus displaying good activity towards cisplatin-resistant cancer cells under both normoxic and hypoxic conditions.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1039/d1cc00258aDOI Listing
April 2021

A novel esterase from a soil metagenomic library displaying a broad substrate range.

AMB Express 2021 Mar 5;11(1):38. Epub 2021 Mar 5.

Institute of Agricultural Applied Microbiology, Jiangxi Academy of Agricultural Sciences, Nanchang, 330200, People's Republic of China.

A novel esterase gene was isolated from a soil metagenomic library. The gene encoded a protein of 520 amino acids which contained a 21 aa signal peptide. Primary structure analysis of the protein sequence revealed that it contained a conserved active site motif (SxSxG) and a structural motif (CS-D-HC). Then the esterase gene was cloned and expressed in Escherichia coli BL21(DE3). SDS-PAGE analysis of the purified esterase showed that it was expressed in a highly soluble form and its molecular mass was estimated to be 55 kDa. Characterization of the esterase revealed that it exhibited high activity toward p-nitrophenyl esters with short acyl chains and especially p-nitrophenyl acetate, suggesting that it was a typical carboxylesterase rather than a lipase. With p-nitrophenyl acetate as substrate, the enzyme showed its optimal activity at pH 7.0 and 30 °C, and it was stable at a broad pH range from 4.5 to 10.0 and temperature not higher than 50 °C. Furthermore, the enzyme showed different substrate specificity from known esterase, it was not only hydrolyzing against p-nitrophenyl esters, but also hydrolyzing all hydroxybenzoic esters and hydroxycinnamic ester assayed. As it was an enzyme active on a broad range of phenolic esters, simultaneously possessing feruloyl esterase, chlorogenate esterase and tannase activities, it could serve as a valuable candidate for applications in biotechnology.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1186/s13568-021-01198-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7936011PMC
March 2021

miR-145-5p attenuates inflammatory response and apoptosis in myocardial ischemia-reperfusion injury by inhibiting NOH-1.

Exp Anim 2021 Mar 4. Epub 2021 Mar 4.

Department of Cardiology, The Second Affiliated Hospital of Shenyang Medical College.

Myocardial ischemia-reperfusion (I/R) injury is a common complication following reperfusion therapy that involves a series of immune or apoptotic reactions. Studies have revealed the potential roles of miRNAs in I/R injury. Herein, we established a myocardial I/R model in rats and a hypoxia/reoxygenation (H/R) model in H9c2 cells and investigated the effect of miR-145-5p on myocardial I/R injury. After 3 h or 24 h of reperfusion, LVESP, EF, and FS were obviously decreased, and LVEDP was increased. Meanwhile, I/R induced an increase in myocardial infarction area. Moreover, a decrease in miR-145-5p and increase in NOH-1 were observed following I/R injury. With this in mind, we performed a luciferase reporter assay and demonstrated that miR-145-5p directly bound to NOH-1 3' UTR. Furthermore, miR-145-5p mimics decreased the levels of TNF-α, IL-1β, and IL-6 via OGD/R stimulation. Upregulation of miR-145-5p increased cell viability and reduced apoptosis accompanied by downregulation of Bax, cleaved caspase-3, cleaved PARP and upregulation of Bcl2. In addition, miR-145-5p overexpression increased SOD activity and reduced ROS and MDA content under OGD/R stress. Notably, NOH-1 could significantly abrogate the above effects, suggesting that it is involved in miR-145-5p-regulated I/R injury. In summary, our findings indicated that miR-145-5p/NOH-1 has a protective effect on myocardial I/R injury by inhibiting the inflammatory response and apoptosis.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1538/expanim.20-0160DOI Listing
March 2021

The modification of a pyrene group makes a Ru(ii) complex versatile.

Chem Commun (Camb) 2021 Apr 2;57(26):3259-3262. Epub 2021 Mar 2.

Laboratory of Photochemical Conversion and Optoelectronic Materials, Technical Institute of Physics and Chemistry, Chinese Academy of Sciences, Beijing 100190, P. R. China.

In this work, the simple modification of a pyrene group on the labile ligand gives the resultant complex 1 versatility, for example, "turn-on" fluorescence after photo-dissociation, dual PDT and PACT activity, and a large two-photon absorption cross section.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1039/d0cc08400jDOI Listing
April 2021

Reductively modified albumin attenuates DSS-Induced mouse colitis through rebalancing systemic redox state.

Redox Biol 2021 May 5;41:101881. Epub 2021 Feb 5.

Divison of Molecular Signaling, Department of the Advanced Biomedical Research, Interdisciplinary Graduate School of Medicine, University of Yamanashi, Chuo, Yamanashi, Japan. Electronic address:

Albumin (Alb) is the most abundant plasma protein with multiple biological functions, including antioxidative property through its thiol activity. Given that inflammatory bowel disease is associated with a decreased level of Alb and an increased level of Alb oxidation, we asked whether Alb could have a therapeutic effect on colitis. Here we tested this possibility. Bovine serum albumin (BSA) was reductively modified with dithiothreitol (DTT) and administrated via gavage or intraperitoneal injection. Dextran sulfate sodium (DSS)-induced mice colitis was associated with massive oxidative stress, as indicated by the elevated sulfenic acid formation in blood, colon tissues, and feces. Treatment of mice with the reductively modified albumin (r-Alb) attenuated the oxidative stress and reduced local inflammation and tissue injury. These effects of r-Alb were only partially achieved by unmodified Alb and wholly lost after blocking the -SH groups with maleimide. In cultured colon epithelial cells, r-Alb prevented DSS- and HO-induced ROS elevation and barrier dysfunction, preceded by inhibition of sulfenic acid formation and P38 activation. Further analysis revealed that Alb was susceptible to HO-induced oxidation, and it detoxified HO in a -SH group-dependent way. Moreover, Alb reacted with GSH/GSSG via thiol-disulfide exchange and reciprocally regulated the availability of -SH groups. Collectively, our study shows that r-Alb effectively attenuates DSS colitis via -SH group-mediated antioxidative action. Given that the oxidative stress underlies many life-threatening diseases, r-Alb, functioning as a potent antioxidant, could have a wide range of applications.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.redox.2021.101881DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7897995PMC
May 2021

SphK1-targeted miR-6784 inhibits functions of skin squamous cell carcinoma cells.

Aging (Albany NY) 2021 01 19;13(3):3726-3741. Epub 2021 Jan 19.

Clinical Laboratory, The Second Affiliated Hospital of Nantong University, Nantong, China.

Sphingosine kinase 1 (SphK1) is overexpressed in skin squamous cell carcinoma (SCC). It has emerged as a novel therapeutic oncotarget. The current study identified a novel SphK1-targeting microRNA, microRNA-6784 (miR-6784). Here, we show that miR-6784 is located at the cytoplasm of A431 skin SCC cells. It directly binds to mRNA. Ectopic overexpression of miR-6784 inhibited 3'-untranslated region (UTR) luciferase activity and downregulated its expression. Moreover, miR-6784 overexpression caused ceramide accumulation in skin SCC cells. Functional studies in established (A431 and SCC9) and primary skin SCC cells revealed that miR-6784 overexpression inhibited cell viability, proliferation, migration, and invasion. It also simultaneously provoked apoptosis activation. Conversely, miR-6784 silencing by antagomiR-6784 induced SphK1 elevation and augmented A431 cell proliferation, migration, and invasion. miR-6784 overexpression-induced anti-A431 cell activity was inhibited by the expression of an UTR-null SphK1 construct. CRISPR/Cas9-induced SphK1 knockout inhibited A431 cell growth. Importantly, miR-6784 was completely ineffective when treating SphK1-knockout A431 cells. Collectively, miR-6784 silences SphK1 and inhibits skin SCC cell progression.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.18632/aging.202336DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7906188PMC
January 2021

Progress in studying heteromorphic leaves in : leaf morphology, anatomical structure, development regulation and their ecological adaptation to arid environments.

Plant Signal Behav 2021 Apr 11;16(4):1870842. Epub 2021 Jan 11.

State Key Laboratory of Crop Biology, College of Life Sciences, Shandong Agricultural University, Taian, China.

Oliv. is a tree that is strongly resistant to drought and salt stress, which is primarily distributed in arid and semiarid lands. The leaves of the species exhibit a special feature that causes them to be designated as heterophylly. In this brief review, we primarily discuss the heteromorphic leaf development and anatomical features, such as the differentiation of spongy and palisade tissues, in heteromorphic leaves of the species. Furthermore, we also discuss the different physiological characteristics in heteromorphic leaves related to the ecological adaptation of to drought environments. These traits in may help researchers evaluate its ecological value in arid areas and evaluate its scientific merit in understanding the mechanism of development of heteromorphic leaves in plants.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1080/15592324.2020.1870842DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7971333PMC
April 2021

Study on thermal expansion characteristics of mixed systems of flaky dust and alkane liquid.

Rev Sci Instrum 2020 Aug;91(8):083901

Beijing Institute of Technology, State Key Laboratory of Explosion Science and Technology, Beijing 100081, China.

To obtain the cubical coefficients of thermal expansion of a mixed system of flaky dust and alkane liquid, the volume and pressure of the mixed system under different temperatures and volume fractions of aluminum powder were measured. On the basis of the experimental results, the cubical coefficients of thermal expansion under the corresponding conditions were calculated and the effect of each influencing factor was obtained. The results show that since the volume of each phase component in the system increases with temperature, the volume of the mixed system also increases with temperature. With increasing temperature, the cubical coefficients of thermal expansion of the mixed system generally increase. Affected by the increase in mass concentration of low-expansion-coefficient substances, an increase in the volume fraction of aluminum powder results in a decrease in the volume thermal expansion coefficient of the mixed system. At the same time, due to the changes in the state of the mixed system, the mass fraction of aluminum powder decreased sharply within a certain range. The low mass fraction of aluminum powder weakens the supporting effect of the metal particle skeleton, the thermal expansion properties of the liquid dominate the mixed system, and the volume thermal expansion coefficient is high. The high aluminum powder mass fraction creates the metal particle skeleton, the metal thermal expansion properties dominate the mixed system, and the volume thermal expansion coefficient is low.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1063/1.5138957DOI Listing
August 2020

Apolipoprotein CIII Deficiency Protects Against Atherosclerosis in Knockout Rabbits.

Arterioscler Thromb Vasc Biol 2020 09 6;40(9):2095-2107. Epub 2020 Aug 6.

From the Department of Molecular Pathology, Faculty of Medicine, Interdisciplinary Graduate School of Medicine, University of Yamanashi, Chuo, Japan (H.Y., M.N., H.Z., Y.C., C.W., J.F.).

Objective: Apo (apolipoprotein) CIII mediates the metabolism of triglyceride (TG)-rich lipoproteins. High levels of plasma apoCIII are positively correlated with the plasma TG levels and increase the cardiovascular risk. However, whether apoCIII is directly involved in the development of atherosclerosis has not been fully elucidated. Approach and Results: To examine the possible roles of apoCIII in lipoprotein metabolism and atherosclerosis, we generated apoCIII KO (knockout) rabbits using ZFN (zinc finger nuclease) technique. On a normal standard diet, apoCIII KO rabbits exhibited significantly lower plasma levels of TG than those of WT (wild type) rabbits while total cholesterol and HDL (high-density lipoprotein) cholesterol levels were unchanged. Analysis of lipoproteins isolated by sequential ultracentrifugation revealed that reduced plasma TG levels in KO rabbits were accompanied by prominent reduction of VLDLs (very-low-density lipoproteins) and IDLs (intermediate-density lipoproteins). In addition, KO rabbits showed faster TG clearance rate after intravenous fat load than WT rabbits. On a cholesterol-rich diet, KO rabbits exhibited constantly and significantly lower levels of plasma total cholesterol and TG than WT rabbits, which was caused by a remarkable reduction of β-VLDLs-the major atherogenic lipoproteins. β-VLDLs of KO rabbits showed higher uptake by cultured hepatocytes and were cleared faster from the circulation than β-VLDLs isolated from WT rabbits. Both aortic and coronary atherosclerosis was significantly reduced in KO rabbits compared with WT rabbits.

Conclusions: These results indicate that apoCIII deficiency facilitates TG-rich lipoprotein catabolism, and therapeutic inhibition of apoCIII expression may become a novel means not only for the treatment of hyperlipidemia but also for atherosclerosis.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1161/ATVBAHA.120.314368DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7484272PMC
September 2020

Gap junctions amplify TRPV4 activation-initiated cell injury via modification of intracellular Ca and Ca-dependent regulation of TXNIP.

Channels (Austin) 2020 12;14(1):246-256

Division of Molecular Signaling, Department of the Advanced Biomedical Research, Interdisciplinary Graduate School of Medicine, University of Yamanashi , Chuo, Japan.

The elevated intracellular Ca and oxidative stress are well-reported mechanisms behind renal tubular epithelial injury initiated by various insults. Given that TRPV4 and connexin43 (Cx43) channels are activated by a wide range of stimuli and regulate both intracellular Ca and redox status, we speculated an involvement of these channels in renal tubular cell injury. Here, we tested this possibility and explored the potential underlying mechanisms. Our results demonstrated that exposure of renal tubular epithelial cells to aminoglycoside G418 led to cell death, which was attenuated by both TRPV4 and gap junction (Gj) inhibitor. Activation of TRPV4 caused cell damage, which was associated with an early increase in Cx43 expression and function. Inhibition of Cx43 with chemical inhibitor or siRNA largely prevented TRPV4 activation-induced cell damage. Further analysis revealed that TRPV4 agonists elicited a rise in intracellular Ca and caused a Ca-dependent elevation in TXNIP (a negative regulator of the antioxidant thioredoxin). In the presence of Gj inhibitor, however, these effects of TRPV4 were largely prevented. The depletion of intracellular Ca with Ca chelator BAPTA-AM or downregulation of TXNIP with siRNA significantly alleviated TRPV4 activation-initiated cell injury. Collectively, our results point to a critical involvement of TRPV4/Cx43 channel interaction in renal tubular cell injury through mechanisms involving a synergetic induction of intracellular Ca and oxidative stress. Channel interactions could be an important mechanism underlying cell injury. Targeting channels could have therapeutic potential for the treatment of acute tubular cell injury.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1080/19336950.2020.1803552DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7515575PMC
December 2020

Cardiac injury after acute carbon monoxide poisoning and its clinical treatment scheme.

Exp Ther Med 2020 Aug 27;20(2):1098-1104. Epub 2020 May 27.

Department of Cardiology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266000, P.R. China.

This study was designed to investigate cardiac injury after acute carbon monoxide poisoning and its clinical treatment scheme. Seventy patients with moderate and severe acute carbon monoxide poisoning (ACOP) admitted from January 2017 to December 2018 into The Affiliated Hospital of Qingdao University were regarded as a research group (RG), and another 30 healthy adults undergoing physical examination in the hospital during the same period were selected as a control group (CG). Thirty-five patients in the RG who received hyperbaric oxygen therapy were considered as group A, and 35 patients who received extracorporeal membrane oxygenation therapy were considered as group B. The effective rates and complications of the two groups after treatment were compared. The concentrations of creatine kinase isoenzyme (CK-MB) and lactate dehydrogenase (LDH) of myocardial enzymes at different time points before and after treatment were detected. Expression of miR-30a in the blood of experimental subjects was detected by time-fluorescence quantitative PCR, and the relationship between miR-30a expression and ACOP patients was analyzed. Patients in groups A and B achieved obvious efficacy, but the effective rate and incidence rate of complications in the extracorporeal membrane oxygenation (ECMO) group were better than those in the hyperbaric oxygen group. The concentrations of CK-MB and LDH in group A and group B were significantly higher than those in control group (P<0.01). The expression level of miR-30a in the RG was significantly higher than that in the control group (P<0.05). Both hyperbaric oxygen therapy and ECMO therapy have obvious efficacy on ACOP patients, but the latter is better than the former. The expression level of miR-30a in blood of ACOP patients increased significantly, which is positively correlated with myocardial injury, and it decreased after treatment. It is believed that miR-30a can provide a reference index for early diagnosis and prediction of disease progression and prognosis in cardiac injury of ACOP.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3892/etm.2020.8801DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7388256PMC
August 2020

A Novel Multi-Focus Image Fusion Network with U-Shape Structure.

Sensors (Basel) 2020 Jul 13;20(14). Epub 2020 Jul 13.

School of Remote Sensing and Information Engineering, Wuhan University, Wuhan 430000, China.

Multi-focus image fusion has become a very practical image processing task. It uses multiple images focused on various depth planes to create an all-in-focus image. Although extensive studies have been produced, the performance of existing methods is still limited by the inaccurate detection of the focus regions for fusion. Therefore, in this paper, we proposed a novel U-shape network which can generate an accurate decision map for the multi-focus image fusion. The Siamese encoder of our U-shape network can preserve the low-level cues with rich spatial details and high-level semantic information from the source images separately. Moreover, we introduce the ResBlocks to expand the receptive field, which can enhance the ability of our network to distinguish between focus and defocus regions. Moreover, in the bridge stage between the encoder and decoder, the spatial pyramid pooling is adopted as a global perception fusion module to capture sufficient context information for the learning of the decision map. Finally, we use a hybrid loss that combines the binary cross-entropy loss and the structural similarity loss for supervision. Extensive experiments have demonstrated that the proposed method can achieve the state-of-the-art performance.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3390/s20143901DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7412084PMC
July 2020

Connexin Hemichannels Contribute to the Activation of cAMP Signaling Pathway and Renin Production.

Int J Mol Sci 2020 Jun 23;21(12). Epub 2020 Jun 23.

Division of Molecular Signaling, Department of the Advanced Biomedical Research, Interdisciplinary Graduate School of Medicine, University of Yamanashi, Chuo 409-3898, Japan.

Connexin hemichannels play an important role in the control of cellular signaling and behaviors. Given that lowering extracellular Ca, a condition that activates hemichannels, is a well-characterized stimulator of renin in juxtaglomerular cells, we, therefore, tested a potential implication of hemichannels in the regulation of renin in As4.1 renin-secreting cells. Lowering extracellular Ca induced hemichannel opening, which was associated with cAMP signaling pathway activation and increased renin production. Blockade of hemichannels with inhibitors or downregulation of Cxs with siRNAs abrogated the activation of cAMP pathway and the elevation of renin. Further analysis revealed that cAMP pathway activation was blocked by adenylyl cyclase inhibitor SQ 22536, suggesting an implication of adenyl cyclase. Furthermore, the participation of hemichannels in the activation of the cAMP signaling pathway was also observed in a renal tubular epithelial cell line NRK. Collectively, our results characterized the hemichannel opening as a presently unrecognized molecular event involved in low Ca-elicited activation of cAMP pathway and renin production. Our findings thus provide novel mechanistic insights into the low Ca-initiated cell responses. Given the importance of cAMP signaling pathway in the control of multiple cellular functions, our findings also highlight the importance of Cx-forming channels in various pathophysiological situations.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3390/ijms21124462DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7353028PMC
June 2020

Zebrafish ubiquitin-specific peptidase 5 (USP5) activates interferon resistance to the virus by increase the expression of RIG-I.

Gene 2020 Aug 11;751:144761. Epub 2020 May 11.

College of Fisheries, Huazhong Agricultural University, Wuhan 430070, China; Hubei Engineering Technology Research Center for Aquatic Animal Diseases Control and Prevention, Wuhan 430070, China. Electronic address:

The ubiquitin specific peptidase (USP) family is involved in many life processes, of which antiviral is also an important basic function. One of the more important ways is to activate interferon. In this study, we reported the antiviral function of the ubiquitin specific peptidase 5(USP5) gene in zebrafish. Evolutionary and comparative protein sequence analysis of the USP5 was performed. The localization of USP5 in FHM cells cytoplasm was determined. Overexpression of USP5 significantly evoked higher expression of mRNA that encode IFNφ1 and ISGs, the promoteractivities of IFNφ1 and IFNstimulated response element (ISRE) were augmented likewise. USP5 was also able to enhance the expression of RIG-I and activate higher levels of IFNφ1 stimulated by Poly (I: C). Viral infection and interference tests demonstrated that USP5 inhibited the replication of SVCV in vitro. In summary, this study reveals that USP5 is able to activate higher levels of interferon by increasing RIG-I protein levels, and thus implement antivirus functions.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.gene.2020.144761DOI Listing
August 2020

Long non‑coding RNA MALAT1 regulates cholesterol accumulation in ox‑LDL‑induced macrophages via the microRNA‑17‑5p/ABCA1 axis.

Mol Med Rep 2020 Apr 13;21(4):1761-1770. Epub 2020 Feb 13.

Department of Cardiology, The Second Affiliated Hospital of Shenyang Medical College, Shenyang, Liaoning 110002, P.R. China.

Atherosclerosis (AS), a major cause of cardiovascular disease, has developed into a serious challenge to the health system. The long non‑coding RNA (lncRNA) metastasis associated lung adenocarcinoma transcript 1 (MALAT1) is associated with the pathogenesis of AS. However, whether MALAT1 can affect cholesterol accumulation in macrophages during AS progression, and the potential molecular mechanism involved in this progression have not been elucidated. In the present study, the mRNA expression level of MALAT1 was measured using reverse transcription‑quantitative PCR (RT‑qPCR) and the protein expression level was detected via western blot analysis. Oil Red O staining was used for detecting lipid accumulation in macrophages. Bioinformatics, dual‑luciferase reporter and RT‑qPCR assays were used to investigate the relationship between MALAT1 and the microRNA (miR)‑17‑5p/ATP‑binding cassette transporter A1 (ABCA1) axis. The present results suggested that the MALAT1 expression level was significantly decreased in patients with AS and in oxidized low‑density lipoprotein (ox‑LDL)‑stimulated macrophages. Knockdown of MALAT1 increased ox‑LDL uptake, lipid accumulation and the total cholesterol (T‑CHO) level in ox‑LDL‑induced macrophages. In addition, MALAT1 inhibition significantly decreased the mRNA and protein expression levels of scavenger receptor (SR) class B member 1, apolipoprotein E (ApoE) and ABCA1. However, MALAT1 increased the expression level of SR class A. Subsequently, the present study investigated whether MALAT1 could target miR‑17‑5p to regulate the expression level of ABCA1, which is involved in cholesterol efflux from macrophages. The present results suggested that inhibition of miR‑17‑5p reversed the effects of MALAT1 knockdown on T‑CHO content, and protein expression levels of ApoE and ABCA1 in ox‑LDL‑stimulated macrophages. In summary, knockdown of MALAT1 may promote cholesterol accumulation by regulating the miR‑17‑5p/ABCA1 axis in ox‑LDL‑induced THP‑1 macrophages.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3892/mmr.2020.10987DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7057819PMC
April 2020

Chlorine and sulfur determination in water using indirect laser-induced breakdown spectroscopy.

Talanta 2020 Jul 19;214:120849. Epub 2020 Feb 19.

Department of Electrical and Computer Engineering, University of Nebraska-Lincoln, Lincoln, NE, 68588-0511, USA.

The detection sensitivity of chlorine (Cl) and sulfur (S) elements is poor using direct laser-induced breakdown spectroscopy (LIBS) because of the high ionization energy of Cl and S. Therefore, a new technique, namely indirect laser-induced breakdown spectroscopy (ID-LIBS), was proposed to improve the detection sensitivity of Cl and S elements. The method detected Cl in water by indirectly detecting the excess silver (Ag) after the precipitation reaction of Ag and chloride. Similarly, the method indirectly detected S in water by detecting the excess barium (Ba) after the precipitation reaction of Ba and sulfate, due to Ag and Ba with low ionization energy and easy excitation. The lines of Ag I 546.5 nm and Ba I 553.5 nm were detected. The R values of 0.999 and 0.997 were obtained for Cl and S, respectively. The limit of quantitation (LoQ) was 2 mg/L for Cl and 5 mg/L for S. The detection sensitivity was improved by about three orders of magnitude compared to using Cl I 822.17 nm and S I 921.28 nm. The results showed that the technique of indirect LIBS can achieve the sensitive detection of Cl and S in water indicating that the technique has tremendous potential for element analysis of water.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.talanta.2020.120849DOI Listing
July 2020

Amide proton transfer-weighted magnetic resonance imaging of human brain aging at 3 Tesla.

Quant Imaging Med Surg 2020 Mar;10(3):727-742

Department of MR, Shandong Medical Imaging Research Institute, Shandong University, Jinan 250021, China.

Background: Amide proton transfer-weighted (APTw) imaging has been revealed to hold great potential in the diagnosis of several brain diseases. The purpose of this proof-of-concept study was to evaluate the feasibility and value of APTw magnetic resonance imaging (MRI) in characterizing normal brain aging.

Methods: A total of 106 healthy subjects were recruited and scanned at 3.0 Tesla, with APTw and conventional magnetization transfer (MT) sequences. Quantitative image analyses were performed in 12 regions of interest (ROIs) for each subject. The APTw or MT ratio (MTR) signal differences among five age groups (young, mature, middle-aged, young-old, and middle-old) were assessed using the one-way analysis of variance, with the Benjamini-Hochberg correction for multiple comparisons. The relationship between APTw and MTR signals and the age dependencies of APTw and MTR signals were assessed using the Pearson correlation and non-linear regression.

Results: There were no significant differences between the APTw or MTR values for males and females in any of the 12 ROIs analyzed. Among the five age groups, there were significant differences in the three white matter regions in the temporal, occipital, and frontal lobes. Overall, the mean APTw values in the older group were higher than those in the younger group. Positive correlations were observed in relation to age in most brain regions, including four with significant positive correlations (r=0.2065-0.4182) and five with increasing trends. As a comparison, the mean MTR values did not appear to be significantly different among the five age groups. In addition, the mean APTw and MTR values revealed significant positive correlations in 10 ROIs (r=0.2214-0.7269) and a significant negative correlation in one ROI (entorhinal cortex, r=-0.2141).

Conclusions: Our early results show that the APTw signal can be used as a promising and complementary imaging biomarker with which normal brain aging can be evaluated at the molecular level.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.21037/qims.2020.02.22DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7136735PMC
March 2020

[Molecular regulative mechanisms of NLRP3 inflammasome activation in diabetic nephropathy and interventional effects of Chinese herbal medicine].

Zhongguo Zhong Yao Za Zhi 2020 Jan;45(1):7-13

Division of Molecular Signaling, Department of Advanced Biomedical Research, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi Yamanashi 409-3898, Japan.

The progression of renal damage in diabetic nephropathy(DN)is closely related to Nod-like receptor protein3(NLRP3)inflammasome activation. The characteristics of NLRP3 inflammasome activation include the changed expression and combination levels of NLRP3, apoptosis-associated speck-like protein(ASC)and pro-caspase-1, the increased expression levels of caspase-1, interleukin(IL)-1β and IL-18 and the excessive release levels of the relative inflammatory mediators. Its molecular regulative mechanisms involve the activation of multiple signaling pathways including reactive oxygen species(ROS)/thioredoxin-interacting protein(TXNIP)pathway, nuclear factor(NF)-κB pathway, nuclear factor erythroid-related factor 2(Nrf2)pathway, long non-coding RNA(lncRNA)pathway and mitogen-activated protein kinases(MAPKs)pathway. In addition, more importantly, never in mitosis aspergillus-related kinase 7(Nek7), as a kinase regulator, could target-combine with NLRP3 at upstream to activate NLRP3 inflammasome. Some extracts of Chinese herbal medicines(CHMs)such as quercetin, curcumin, cepharanthine, piperine and salidroside, as well as Chinese herbal compound prescriptions such as Wumei Pills both could treat NLRP3 inflammasome to ameliorate inflammatory renal damage in DN. Therefore, accurately clarifying the targets of anti-inflammatory CHMs and Chinese herbal compound prescriptions delaying DN progression by targeting the molecular regulative mechanisms of NLRP3 inflammasome activation will be one of the development directions in the future.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.19540/j.cnki.cjcmm.20190618.402DOI Listing
January 2020

Hydrogen Sulfide Mediates Tumor Cell Resistance to Thioredoxin Inhibitor.

Front Oncol 2020 10;10:252. Epub 2020 Mar 10.

Division of Molecular Signaling, Department of the Advanced Biomedical Research, Interdisciplinary Graduate School of Medicine, University of Yamanashi, Kofu, Japan.

Thioredoxin (Trx) is a pro-oncogenic molecule that underlies tumor initiation, progression and chemo-resistance. PX-12, a Trx inhibitor, has been used to treat certain tumors. Currently, factors predicting tumor sensitivity to PX-12 are unclear. Given that hydrogen sulfide (HS), a gaseous bio-mediator, promotes Trx activity, we speculated that it might affect tumor response to PX-12. Here, we tested this possibility. Exposure of several different types of tumor cells to PX-12 caused cell death, which was reversely correlated with the levels of HS-synthesizing enzyme CSE and endogenous HS. Inhibition of CSE sensitized tumor cells to PX-12, whereas addition of exogenous HS elevated PX-12 resistance. Further experiments showed that HS abolished PX-12-mediated inhibition on Trx. Mechanistic analyses revealed that HS stimulated Trx activity. It promoted Trx from the oxidized to the reduced state. In addition, HS directly cleaved the disulfide bond in PX-12, causing PX-12 deactivation. Additional studies found that, besides Trx, PX-12 also interacted with the thiol residues of other proteins. Intriguingly, HS-mediated cell resistance to PX-12 could also be achieved through promotion of the thiol activity of these proteins. Addition of HS-modified protein into culture significantly enhanced cell resistance to PX-12, whereas blockade of extracellular sulfhydryl residues sensitized cells to PX-12. Collectively, our study revealed that HS mediated tumor cell resistance to PX-12 through multiple mechanisms involving induction of thiol activity in multiple proteins and direct inactivation of PX-12. HS could be used to predict tumor response to PX-12 and could be targeted to enhance the therapeutic efficacy of PX-12.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3389/fonc.2020.00252DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7078679PMC
March 2020

Zebrafish NIK Mediates IFN Induction by Regulating Activation of IRF3 and NF-κB.

J Immunol 2020 04 17;204(7):1881-1891. Epub 2020 Feb 17.

College of Fisheries, Huazhong Agricultural University, Wuhan 430070, Hubei, China;

Type I IFN mediates the innate immune system to provide defense against viral infections. NF-B-inducing kinase (NIK) potentiates the basal activation of endogenous STING, which facilitates the recruitment of TBK1 with the ectopically expressed IRF3 to induce IFN production. Moreover, NIK phosphorylates IKKα and confers its ability to phosphorylate p100 (also known as NF-κB2) in mammals. Our study demonstrated that NIK plays a critical role in IFN production in teleost fish. It was found that NIK interacts with IKKα in the cytoplasm and that IKKα phosphorylates the NIK at the residue Thr, which is different from the mammals. Overexpression of NIK caused the activation of IRF3 and NF-κB, which in turn led to the production of IFN and IFN-stimulated genes (ISGs). Furthermore, the ectopic expression of NIK was observed to be associated with a reduced replication of the fish virus, whereas silencing of endogenous NIK had an opposite effect in vitro. Furthermore, NIK knockdown significantly reduced the expression of IFN and key ISGs in zebrafish larvae after spring viremia of carp virus infection. Additionally, the replication of spring viremia of carp virus was enhanced in NIK knockdown zebrafish larvae, leading to a lower survival rate. In summary, our findings revealed a previously undescribed function of NIK in activating IFN and ISGs as a host antiviral response. These findings may facilitate the establishment of antiviral therapy to combat fish viruses.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.4049/jimmunol.1900561DOI Listing
April 2020

Protein-based amide proton transfer-weighted MR imaging of amnestic mild cognitive impairment.

Neuroimage Clin 2020 27;25:102153. Epub 2019 Dec 27.

Department of MR, Shandong Medical Imaging Research Institute, Shandong University, Jinan, Shandong, China. Electronic address:

Amide proton transfer-weighted (APTw) MRI is a novel molecular imaging technique that can noninvasively detect endogenous cellular proteins and peptides in tissue. Here, we demonstrate the feasibility of protein-based APTw MRI in characterizing amnestic mild cognitive impairment (aMCI). Eighteen patients with confirmed aMCI and 18 matched normal controls were scanned at 3 Tesla. The APTw, as well as conventional magnetization transfer ratio (MTR), signal differences between aMCI and normal groups were assessed by the independent samples t-test, and the receiver-operator-characteristic analysis was used to assess the diagnostic performance of APTw. When comparing the normal control group, aMCI brains typically had relatively higher APTw signals. Quantitatively, APTw intensity values were significantly higher in nine of 12 regions of interest in aMCI patients than in normal controls. The largest areas under the receiver-operator-characteristic curves were 0.88 (gray matter in occipital lobe) and 0.82 (gray matter in temporal lobe, white matter in occipital lobe) in diagnosing aMCI patients. On the contrary, MTR intensity values were significantly higher in only three of 12 regions of interest in the aMCI group. Additionally, the age dependency analyses revealed that these cross-sectional APTw/MTR signals had an increasing trend with age in most brain regions for normal controls, but a decreasing trend with age in most brain regions for aMCI patients. Our early results show the potential of the APTw signal as a new imaging biomarker for the noninvasive molecular diagnosis of aMCI.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.nicl.2019.102153DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6948365PMC
December 2020

MicroRNA-421 improves ischemia/reperfusion injury via regulation toll-like receptor 4 pathway.

J Int Med Res 2020 Mar 18;48(3):300060519871863. Epub 2019 Dec 18.

Department of Emergency Medicine, The Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, China.

Objectives: The objective was to investigate the effects of microRNA-421 against myocardial ischemia/reperfusion injury in C57BL/6 mice.

Methods: Male C57BL/6 mice (n = 27) were randomly divided into three groups: normal control (NC) group (sham-treated); I/R model group, which underwent the I/R model (ischemia for 30 minutes followed by reperfusion for 24 hours); and the miRNA group, which were injected with miR-421. Pathology was assessed by hematoxylin and eosin staining and myocardial infarct size was measured by triphenyltetrazolium chloride staining. The apoptosis rate was measured by TUNEL assay, and relative expression of toll-like receptor-4 (TLR4), Janus kinase 2 (JAK2), and signal transducer and activator of translation 3 (STAT3) was evaluated by immunohistochemistry. Interleukin (IL)-6, tumor necrosis factor (TNF)-α, IL-10, and high mobility group protein B1 (HMGB1) serum concentrations were measured by ELISA.

Results: Compared with the NC group, in the model group, the myocardial infarction was large; inflammatory cell infiltration was severe; apoptosis was enhanced; expression of TLR4, JAK2, and STAT3 was increased; and serum concentrations of IL-6, TNF-α, IL-10, and HMGB1 were significantly increased. In the miRNA group, the ischemia/reperfusion injury was significantly improved.

Conclusions: Overexpression of miRNA-421 could reduce ischemia/reperfusion inflammatory response, perhaps via inactivation of TLR4, JAK2, and STAT3.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1177/0300060519871863DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7607211PMC
March 2020

The safety and efficacy of 2% vitamin C solution spray for relief of mucosal irritation caused by Lugol chromoendoscopy: a multicenter, randomized, double-blind, parallel trial.

Gastrointest Endosc 2020 09 26;92(3):554-564. Epub 2019 Nov 26.

Department of Gastroenterology, First Affiliated Hospital of Nanjing Medical University, Nanjing, China; First Clinical Medical College of Nanjing Medical University, Nanjing, China.

Background And Aims: Lugol chromoendoscopy facilitates endoscopic visualization of esophageal dysplasia and carcinoma. Vitamin C solution (VCS) can theoretically neutralize free iodine, which causes mucosal irritation. The aim was to assess the safety and efficacy of VCS for relieving adverse symptoms caused by Lugol iodine staining.

Methods: Two hundred forty eligible patients were randomized to receive 20 mL of normal saline solution (NS), 5% sodium thiosulfate solution (STS), or 2% VCS after spraying 10 mL of 2% Lugol iodine solution on the mid-distal esophagus. The primary endpoints were statistically significant reductions in acute and late adverse symptom severity scores. The secondary endpoint was the discoloration effect on esophageal brown iodine-stained mucosa.

Results: Spraying both VCS and STS similarly decreased the severity scores of acute (NS vs VCS = 2.58 vs 1.61, P = .040; VCS vs STS = 1.61 vs 1.89, P > .999) and late (NS vs VCS = 1.70 vs 0.91, P = .002; VCS vs STS = 0.91 vs 1.38; P = .212) adverse symptoms after Lugol chromoendoscopy compared with spraying NS. Compared with STS spray, VCS spray alleviated acute acid regurgitation or heartburn (33% vs 15%, P = .017) and late retrosternal discomfort or pain (21% vs 9%, P = .027). Moreover, compared with spraying NS, spraying VCS quickly discolored the iodine-stained mucosa, with a better decolorization score (2.26 vs 3.56, P = .000), and the effects of fading iodine dye were similar between VCS and STS (3.56 vs 3.59, P = .908).

Conclusions: VCS can reduce mucosal irritation symptoms induced by Lugol chromoendoscopy and can be routinely recommended. (Chinese Clinical Trial Registry number: ChiCTR1900022000.).
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.gie.2019.11.028DOI Listing
September 2020

Connexin43 Is Required for the Effective Activation of Spleen Cells and Immunoglobulin Production.

Int J Mol Sci 2019 Nov 18;20(22). Epub 2019 Nov 18.

Division of Molecular Signaling, Department of the Advanced Biomedical Research, Interdisciplinary Graduate School of Medicine, University of Yamanashi, Chuo 409-3898, Japan.

Gap junctions (Gjs), formed by specific protein termed connexins (Cxs), regulate many important cellular processes in cellular immunity. However, little is known about their effects on humoral immunity. Here we tested whether and how Gj protein connexin43 (Cx43) affected antibody production in spleen cells. Detection of IgG in mouse tissues and serum revealed that wild-type (Cx43) mouse had a significantly higher level of IgG than Cx43 heterozygous (Cx43) mouse. Consistently, spleen cells from Cx43 mouse produced more IgG under both basal and lipopolysaccharide (LPS)-stimulated conditions. Further analysis showed that LPS induced a more dramatic activation of ERK and cell proliferation in Cx43 spleen cells, which was associated with a higher pro-oxidative state, as indicated by the increased NADPH oxidase 2 (NOX2), TXNIP, p38 activation and protein carbonylation. In support of a role of the oxidative state in the control of lymphocyte activation, exposure of spleen cells to exogenous superoxide induced Cx43 expression, p38 activation and IgG production. On the contrary, inhibition of NOX attenuated the effects of LPS. Collectively, our study characterized Cx43 as a novel molecule involved in the control of spleen cell activation and IgG production. Targeting Cx43 could be developed to treat certain antibody-related immune diseases.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3390/ijms20225789DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6888161PMC
November 2019

Aptamer-antibody dual probes on single-walled carbon nanotube bridged dielectrode: Comparative analysis on human blood clotting factor.

Int J Biol Macromol 2020 May 16;151:1133-1138. Epub 2019 Nov 16.

Department of Hematology, Jinan Central Hospital Affiliated to Shandong University, No. 105, Jiefang Road, Lixia District, Jinan, Shandong Province 250013, PR China. Electronic address:

Haemophilia is a blood clotting disorder known as 'Christmas disease' caused when the blood has defect with the clotting factor(s). Bleeding leads various issues, such as chronic pain, arthritis and a serious complication during the surgery. Identifying this disease is mandatory to take the necessary treatment and maintains the normal clotting. It has been proved that the level of factor IX (FIX) is lesser with haemophilia patient and the attempt here is focused to quantify FIX level by interdigitated electrode (IDE) sensor. Single-walled carbon nanotube (SWCNT) was utilized to modify IDE sensing surface. On this surface, dual probing was evaluated with aptamer and antibody to bring the possible advantages. The detection limit with antibody was found to be 1 pM, while aptamer shows 100 fM. Further, a fine-tuning was attempted with sandwich pattern of aptamer-FIX-antibody and antibody-FIX-aptamer and compared. Specific elevation of detection with 10 folds was noticed and displayed the detection at 100 f. in both sandwich patterns. In addition, FIX was detected in the diluted human serum by aptamer-FIX-antibody sandwich, it was found that FIX detected from the dilution factor 1:640. A novel demonstration is with higher discrimination against other clotting factors, XI and VII.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.ijbiomac.2019.10.156DOI Listing
May 2020

Demonstration of a Timescale Based on a Stable Optical Carrier.

Phys Rev Lett 2019 Oct;123(17):173201

JILA, NIST and University of Colorado, 440 UCB, Boulder, Colorado 80309, USA.

We report on the first timescale based entirely on optical technology. Existing timescales, including those incorporating optical frequency standards, rely exclusively on microwave local oscillators owing to the lack of an optical oscillator with the required frequency predictability and stability for reliable steering. We combine a cryogenic silicon cavity exhibiting improved long-term stability and an accurate ^{87}Sr lattice clock to form a timescale that outperforms them all. Our timescale accumulates an estimated time error of only 48±94  ps over 34 days of operation. Our analysis indicates that this timescale is capable of reaching a stability below 1×10^{-17} after a few months of averaging, making timekeeping at the 10^{-18} level a realistic prospect.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1103/PhysRevLett.123.173201DOI Listing
October 2019

Meta-analysis of vitamin D and lung function in patients with asthma.

Respir Res 2019 Oct 8;20(1):161. Epub 2019 Oct 8.

Department of Intensive Care Unit, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang Province, China.

Background: There is growing literature suggesting a link between vitamin D and asthma lung function, but the results from systematic reviews are conflicting. We conducted this meta-analysis to investigate the relation between serum vitamin D and lung function in asthma patients.

Methods: Major databases, including OVID, MEDLINE, Web of Science and PUBMED, were searched until 10th October 2018. All published observational studies related to vitamin D and asthma were extracted. All meta-analyses were performed using Review Manager 5.3.5.

Results: This quantitative synthesis found that asthma patients with low vitamin D levels had lower forced expiratory volume In 1 s (FEV1) (mean difference (MD) = - 0.1, 95% CI = - 0.11 to - 0.08,p < 0.01;I2 = 49%, p = 0.12) and FEV1% (MD = - 10.02, 95% CI = - 11 to - 9.04, p < 0.01; I2 = 0%, p = 0.82) than those with sufficient vitamin D levels. A positive relation was found between vitamin D and FEV1 (r = 0.12, 95% CI = 0.04 to 0.2, p = 0.003; I2 = 59%,p = 0.01), FEV1% (r = 0.19, 95% CI = 0.13 to 0.26, p < 0.001; I2 = 42%, p = 0.11), forced vital capacity (FVC) (r = 0.17, 95% CI = 0.00 to 0.34, p = 0.05; I2 = 60%, p = 0.04), FEV1/FVC (r = 0.4, 95% CI = 0.3 to 0.51, p < 0.001; I2 = 48%, p = 0.07), and the asthma control test (ACT) (r = 0.33, 95% CI = 0.2 to 0.47, p < 0.001; I2 = 0%, p = 0.7). Subgroup analysis indicated that the positive correlation between vitamin D and lung function remained significant in both children and adults.

Conclusions: Our meta-analysis suggested that serum vitamin D levels may be positively correlated with lung function in asthma patients. Future comprehensive studies are required to confirm these relations and to elucidate potential mechanisms.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1186/s12931-019-1072-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6781357PMC
October 2019